Participation of Hepatic Glucoreceptors in the Control of Intake of Food

Russek, M.

doi:10.1038/197079b0

Cited by 255 publications

(95 citation statements)

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“…5 Its activation stimulates first-phase insulin secretion, 16,17 increases hepatic glucose clearance, 18 stimulates, in an insulin-independent manner, peripheral tissue glucose uptake, 8,19 suppresses glucagon secretion (see below) and terminates feeding. 20,21 Thus, the combination of physiological as well as pharmacological and genetic studies has provided strong evidence for an important role of the hepatoportal sensor in the regulation of several homeostatic functions. These studies indicate that glucose sensing in the portal vein not only shares similarity with that of the pancreatic beta-cell but also has differences, particularly the capacity to be activated by pyruvate and lactate.…”

Section: Sites and Mechanisms Of Glucose Sensingmentioning

confidence: 99%

“…74 On the other hand, the induction of cellular glucoprivation by intraperitoneal or intracerebroventricular administration of the glucose anti-metabolite 2-DG is a strong signal to induce food intake. [75][76][77] Glucose sensing in metabolic diseases B Thorens A possible role of the hepatoportal vein sensor in the glucose regulation of feeding was proposed in initial studies by Russek,20,21 who showed that intraperitoneal glucose injection in the rat rapidly decreased feeding, an effect attributed to glucose inducing a satiety signal after being collected in the portal vein. In addition, portal vein infusion of glucose inhibits, 78 whereas 2-DG stimulates 75 feeding and intrameal portal glucose infusion increases satiation in the rat.…”

Section: Feeding Controlmentioning

confidence: 99%

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Glucose sensing and the pathogenesis of obesity and type 2 diabetes

Thorens

2008

Int J Obes

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The control of body weight and of blood glucose concentrations depends on the exquisite coordination of the function of several organs and tissues, in particular the liver, muscle and fat. These organs and tissues have major roles in the use and storage of nutrients in the form of glycogen or triglycerides and in the release of glucose or free fatty acids into the blood, in periods of metabolic needs. These mechanisms are tightly regulated by hormonal and nervous signals, which are generated by specialized cells that detect variations in blood glucose or lipid concentrations. The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Other signaling molecules, such as the adipocyte hormones leptin and adiponectin, have circulating plasma concentrations that reflect the level of fat stored in adipocytes. These signals are integrated at the level of the hypothalamus by the melanocortin pathway, which produces orexigenic and anorexigenic neuropeptides to control feeding behavior, energy expenditure and glucose homeostasis. Work from several laboratories, including ours, has explored the physiological role of glucose as a signal that regulates these homeostatic processes and has tested the hypothesis that the mechanism of glucose sensing that controls insulin secretion by the pancreatic beta-cells is also used by other cell types. I discuss here evidence for these mechanisms, how they integrate signals from other nutrients such as lipids and how their deregulation may initiate metabolic diseases.

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Section: Sites and Mechanisms Of Glucose Sensingmentioning

confidence: 99%

Section: Feeding Controlmentioning

confidence: 99%

Glucose sensing and the pathogenesis of obesity and type 2 diabetes

Thorens

2008

Int J Obes

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“…Russek postulated the presence of glucose receptors in the liver and formulated the hepatostatic theory of EB regulation (Russek, 1963) Flatt extended these High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S157 models and evolved the glycogenostatic model of appetite regulation, which is based on the notion that CHO stores (which are related to CHO intake) exert negative feedback on EI (Flatt, 1987).…”

Section: Appetite Control Mechanisms Which Limit Cho and Fat Intakesmentioning

confidence: 99%

High and low carbohydrate and fat intakes: limits imposed by appetite and palatability and their implications for energy balance

Blundell

Stubbs²

1999

Eur J Clin Nutr

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This report examines several issues concerning the effects of dietary fats and carbohydrates (CHOs) on body weight and the limits set on the intake of these nutrients by factors in¯uencing appetite control: (i) the physiological relationship between feeding behaviour (FB) and body weight; (ii) the distribution of nutrients in Western foods and the implications this may have for FB; (iii) the contribution of nutrients in the diet, to total EI under both extreme and typical Western conditions; (iv) the known effects that fats, CHOs and dietary energy density (ED) exert on appetite and energy balance (EB); (v) the potential role of sensory factors in promoting or limiting fat, CHO and energy intakes (EI) in modern human populations Population studies and large surveys have identi®ed individuals with wide ranges of fat and CHO intakes. Intakes of fat can vary from an average of 180 gaday to 25 gaday in a representative sample. But on individual days fat intake can rise to well over 200 g according to a selection of high fat foods. In a single meal, people can consume an amount of fat greater than the population daily average. From this analysis it can be deduced that the appetite control mechanism will permit the consumption of large amounts of fat (if an abundance of high fat foods exist in the food supply). Except for speci®c physiological circumstances (e.g. endurance explorers) where there is an urgent need for EIs, in the face of decreasing body weight, it is unlikely that the body will generate a speci®c drive for fat. Because CHO foods have a lower ED than fat foods (on average) and because of their greater satiating capacity, the free intake of high CHO foods is likely to be self-limiting (at lower EIs than those generated by fatty foods). This does not mean that excess EIs are impossible when people feed ad libitum on high CHO diets.

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“…In our study we can assume that the U 13 C 6 glucose appears in the systemic circulation slightly later than any appearance of glucose in the portal system, indicating a positive portal arterial glucose concentration gradient at the time of inducing hypoglycaemia as the tracer levels in the circulation are increasing. Portal-arterial glucose gradients have been implicated in the control of net hepatic glucose uptake [38,39,40], food intake [41], and recently tissue glucose utilisation [42]. Alternatively, any effects we observed could have been a direct result of changes in stimulus to the portal vein glucose sensors themselves.…”

Section: Discussionmentioning

confidence: 89%

“…This could relate to the reduced adrenaline responses but the size of the effect on neuroglycopenic as well as autonomic symptoms suggests additional mechanisms are involved. The portal signal can control food intake independent of catecholamines [41]. The lateral hypothalamus contains glucose-sensitive neurones that are stimulated by hypoglycaemia indirectly [47] via signals transmitted from the nucleus tractus solitarius [48].…”

Section: Discussionmentioning

confidence: 99%

The role of hepatic portal glucose sensing in modulating responses to hypoglycaemia in man

et al. 2002

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Aims/hypothesis. The role of glucose sensing cells in the human hepatic portal system in the initiation of the neuroendocrine responses to acute hypoglycaemia is not known. We investigated the effect of raising blood glucose concentrations in the hepatic-portal vein on neurohumoral responses during induction of systemic hypoglycaemia in nine healthy male volunteers. Methods. Each subject received an insulin infusion (3 mU·kg -1 ·min -1 ) on two occasions, in random order. Variable rate glucose infusion was used to maintain plasma glucose at 5 mmol/l for 60 min, then 3.2 mmol/l for 60 min. At 20 min prior to hypoglycaemia, subjects drank 20 g of glucose in water or water sweetened with saccharin. In five of the volunteers, the oral glucose was labelled with U-13C6 glucose, which showed peak systemic glucose absorption between 90 and 110 min. Five volunteers also repeated the study with a euglycaemic clamp.Results. Oral glucose was associated with a reduction in the early adrenaline response to hypoglycaemia, the area under the curve from 90 to 110 min falling from 24.02±20.84 (means ± SD) to 15. vere hypoglycaemia during the pharmacological treatment of diabetes mellitus. The inability to generate or detect the warning symptoms of early hypoglycaemia puts diabetic patients at high risk of episodes of severe hypoglycaemia [1] and often the fear of hypoglycaemia limits the optimisation of glycaemic control [2]. Associated with loss of subjective awareness of hypoglycaemia is a lowering of the glucose concentration required to initiate the counterregulatory response to hypoglycaemia, as well as a reduction in the magnitude and intensity of the counterregulatory response at any given blood glucose concentration [3,4,5]. The speculation that these defects are principally the result of defective glucose sensing gains support from data showing similar changes in the neuroendocrine rePerception of a minor decrease in plasma glucose concentration and initiation of a counterregulatory response are essential factors in the defence against se-

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Participation of Hepatic Glucoreceptors in the Control of Intake of Food

Cited by 255 publications

References 1 publication

Glucose sensing and the pathogenesis of obesity and type 2 diabetes

Glucose sensing and the pathogenesis of obesity and type 2 diabetes

High and low carbohydrate and fat intakes: limits imposed by appetite and palatability and their implications for energy balance

The role of hepatic portal glucose sensing in modulating responses to hypoglycaemia in man

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